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Abstract
A number of neuroendocrine changes have been described after stroke, which may serve adaptive or deleterious functions. The neuroendocrine changes include activation of the hypothalamo–pituitary–adrenal axis, sympathetic nervous system and alterations of several hormonal levels. Alterations of the HPA axis, increased catecholamines, natriuretic peptides and, decreased melatonin and IGF-1 levels are associated with poor post-stroke outcome, although there is no definitive proof of causality. Therefore, it remains to be established whether alteration of neuroendocrine responses could be used as a potential therapeutic target to improve stroke outcome. This article gives an overview of the major neuroendocrine pathways altered by stroke and highlights their potential for clinical use and further neurotherapeutic development by summarizing the evidence for their association with stroke outcome including functional outcome, post-stroke infection, delirium, depression and stroke-related myocardial injury.
Acknowledgements
The authors would like to thank E Bennett for critical review of the manuscript.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Key issues
Following stroke, neuroendocrine changes include activation of the hypothalamo–pituitary–adrenal axis, sympathetic nervous system and alterations in the levels of several hormones including natriuretic peptides, melatonin and IGF-1. Different alterations of these pathways seem to be associated not only with functional outcome and mortality, but also with post-stroke infection, depression and disturbance in cognition.
The hormonal response to stroke is modulated by interacting cytokines, metabolic derangements, concurrent infection, fever, medications, age, comorbidities and physiologic hormonal fluctuation. These factors should be accounted for when interpreting or planning for neuroendocrine studies post-stroke.
Natriuretic peptides typically increase following stroke. Elevated levels are associated with poor outcome. This relationship could be due to an adaptive response rather than a direct deleterious effect.
Copeptin is more easily measured than adrenocorticotropic hormone and cortisol, demonstrates less variability and correlates well with stroke outcome. Owing to these characteristics, it represents a reasonable candidate for future development as a marker for stroke prognosis. More studies are needed to determine if the increase in copeptin post-stroke is adaptive or deleterious.
Melatonin is decreased following stroke, but its role in the pathophysiology of depressive symptoms and sleep disturbance following stroke requires further investigation.
Alterations in the hypothalamo–pituitary–adrenal following stroke is associated with increased risk for infection, depression and delirium.
In clinical practice, none of the neuroendocrine biomarkers described in this review are currently indicated for use in stroke prognosis. Additional studies are necessary to determine their role above and beyond current prognostic tools such as stroke severity and age.
Neuroendocrine pathways play an important role in determining the multiple facets of stroke outcome and are likely to continue to be targets of future studies of biomarker validation in stroke prognosis and potential new therapies.